Once, when I was a night intern presenting to the day team an admission, I was questioned, then berated, regarding my management regarding hyperkalemia. Mild hyperkalemia. The specifics of the case I don’t remember. However, I remember running through the presentation:

Labs: Sodium normal Potassium 5.5 mEq/L, for which we gave 15 grams of kayexalate…

The patient didn’t have any reason for the hyperkalemia. None of the classic effects of a potassium sparing diuretic, renal failure, or the surreptitious – or not so surreptitious – use of an angiotensin converting enzyme inhibitor. The patient had plain, ol’ hyperkalemia. The red blood cells in the sample had not hemolyzed, or ruptured releasing all of their intracellular potassium stores and falsely elevating extracellular concentrations of potassium – more on this later. And, the patient’s heart had not ceased beating from a cataclysmic change in cardiac myocyte action potentials.

As I attempted to continue my presentation. I was stopped by the attending – the king of my medical audience, “What else did you do for the potassium?” I was puzzled.

I errr gave kayexalate…(Damn, I just said that.. There must be something I am missing. Did he want me to load this patient up with other medications… The potassium was only 5.5, only 0.5 mEq/L above the upper limit of normal. Only a 10% change from being normal!)

Most people would say that clinically relevant, or moderate hyperkalemia, doesn’t start until 6.0 mEq/L or higher. Normal potassium being between 3.5 and 5.0 mEq/L plus minus a few. Life in the Fast Lane, a popular website for those within the emergency medicine circle and close-by, does not classify hyperkalemia until it is greater than 5.5 mEq/L – an upper limit that would have allowed me to pedal my way through my admission presentation without questioning and sooner to sleeping.1 Alas, my attending probably had neither visited the website nor cared to, I assume.

Management techniques vary from administering beta-2 agonists, like albuterol, to the combined administration of insulin with dextrose – all of which abscond potassium into the cells of the body and away from the all-important cell membrane of the heart, but only for a short period of time. After a couple hours, the potassium re-emerges from the body’s intracellular storehouses as the effects of albuterol and dextrose abate. The only way to truly remove potassium from the blood is to remove it from the body, either by peeing it out or pooping it out. Bodily excretion is facilitated renally by the water pill furosemide and gastrointestinally by the potassium binding resin kayexalate. In some emergent cases, potassium can be removed by dialysis.

The danger with moderate or severe (> 7.0 mEq/L) hyperkalemia is the genesis of fatal, cardiac arrhythmias, whose non-fatal progenitors can be seen on electrocardiograms by the creation and absence of peaks in places where there shouldn’t be any. As I learned in the ensuing seconds of my presentation, my transgression was in my failure to obtain an EKG. I never obtained the electrocardiographic tracing because of the reported lack of seeing anything with such mild elevations. Most medical students learn that the earliest changes can be seen with serum concentrations starting at 6.0 mEq/L, assuming the other electrolytes are in order. Regardless of the appropriateness, I had forever been molded to get an EKG for a serum potassium level 5.5 mEq/L.

Months later, I found myself dealing with mission creep when a different patient’s serum potassium level was 5.4 mEq/L. Do I get an EKG now? Reminiscing of Catch-22’s Captain Yossarian, I found myself wondering if 0.1 mEq/L made all the difference between when I would get an EKG on a patient or not. If 5.4 mEq/L was high enough, then what about 5.3 mEq/L? 5.2 mE/L? As the resident on the team this time, I had an intern that I could defer to management and override as I saw appropriate, as the attending had done to me earlier.

“I gave him 15 grams of kayexlate,” my intern said. 15 grams of kayexalate, or sodium polystyrene, was enough to lower his potassium to a theoretical level of 4.4-4.6 mEq/L based on nearly five decades of experience since its first use and in accordance with American Heart Association guidelines.2,3 For some fateful reason, I found myself looking at the actual lab report of the patient’s electrolytes and found the archetypal asterisk next to the potassium measurement. It had marked the sample as hemolyzed – the potassium level measured was higher than the patient’s true serum potassium level. The patient’s potassium level could have been normal, or even low, and giving a medication to lower serum potassium levels further could have been just as unfortunate as having too high a potassium. I felt knowledgeable educating my naïve intern about the subtle asterisks trailing lab reports. More importantly, I was relieved that I didn’t have to deal with the vexing question of whether to get an EKG for mild hyperkalemia.
Mid-way through residency, however, I could not escape the question. I found myself with another intern treating the same serum potassium level of 5.4 mEq/L on an entirely different patient. This time the patient’s measurement had not been hemolyzed. Feeling anally-retentive, I ordered an EKG and gave kayexalate. Probably both of which were unnecessary, but I had been pre-programmed by my previous experience to obtain EKGs in mild hyperkalemia. And, I could not make the same mistake twice.

As my intern was presenting our management, he met a cavalcade of criticisms for now over-testing and over-treating mild hyperkalemia. I jumped in, blurting

I just wanted to be sure that we didn’t…

My attending cut me off with the same fervor the previous attending months ago had for doing the exact opposite management for nearly the same situation. I felt like I was in the twilight zone. Or the hospital of Catch-22. I was the Captain Yossarian of medicine. The situation left me wondering if 5.4 mEq/L was all that different from 5.5 mEq/L? Or not? Our attending this time was content to have mild hyperkalemia and would have preferred us not to have given the kayexalate or ordered an EKG. True, kayexalate has the rare and unpleasant side effect of intestinal necrosis requiring emergent surgery, and an EKG can lead to more testing and intervention than otherwise would have been necessary.4 We as a medical team also had more pressing issues, like the persistence of a fever in the other patient across the hall. But probably the biggest reason to not intervene would be because mild hyperkalemia is called mild for a reason. The best course of action would be to repeat labs the next morning, or perhaps earlier if one was absolutely concerned that the serum potassium level was rising.

The differences in management within healthcare can be considered to be the so called “art of medicine.” However, to borrow another adage, beauty is in the eye of the beholder. To some, the varied and polar managements in the same setting might be called the “craziness of medicine.” This is repeated over and over in many other situations, like the physician’s preference for PSA testing in older men. For more permanent and serious issues, it is worthwhile to include the patient in the discussion and have them pick their management. In the age of ever-increasing patient awareness and involvement, some would argue that I should have presented the various treatment strategies with all of their associated risks, benefits, and alternatives and allowed the patient to make an informed decision for mild hyperkalemia. In effect, I would be consenting the patient for a minor electrolyte abnormality, but patient-centered decision making will always trump physician-centered decision as we, as a medical community, have made a conscientious effort to value patient autonomy. However, if we started doing this for mild hyperkalemia, where would it stop? Would we consent patients for the blood draw to check the electrolytes in the first place? A blood draw, or venipuncture, gone wrong can cause a hematoma, an abscess, thrombophlebitis, a blood infection, and worse when one patient’s blood is mislabeled as another and physicians then treat the wrong patient. The possibilities of the risks are endless. To consent for everything individually would bring healthcare to a halt. Hospitals have circumvented this by consenting patients for most “non-major” things with a general consent. Patients are consented for treatment upon admission with some variant of a “General Consent for Treatment” form that most of us usually don’t pay attention because it doesn’t explain the details of something like the treatment of mild hyperkalemia.

In the end, attending physicians will have their own personal preferences towards medical management. Their preference is a product of their learning and experience, which may have been as confusing and contradictory as their residents’. When following suit, we should understand their choices as best we can, even if they are at odds with what we have learned in the months or days prior. Someday, we will be attendings of our own and be making our own decisions. Some of us will even have our own interns and residents to guide. In the future, I will only observe a potassium of 5.4 mEq/L but likely intervene for a potassium of 5.5 mEq/L.